Unique molecular signatures typify skin inflammation induced by chemical allergens and irritants
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ABSTRACT:
PROVIDER: PRJNA713803 | ENA |
REPOSITORIES: ENA
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Project description:A transcriptomic comparative analysis was performed to explore and characterize the molecular signatures of chemical-induced skin inflammation, in order to identify biomarkers that could discriminate allergic from irritant contact dermatitis.
2021-04-12 | GSE168735 | GEO
Project description:Epigenetic regulation of gene expression plays a pivotal role in the orchestration of immune responses and may determine the vigor, quality, or longevity of such responses. Chemical allergens can be divided into two categories: skin sensitizing chemicals associated with allergic contact dermatitis, and chemicals that cause sensitization of the respiratory tract and occupational asthma. In mice these are characterized by different T helper (Th) cell responses. To explore the regulation and maintenance of these divergent responses, mice were exposed to 2,4-dinitrochlorobenzene (DNCB; a contact allergen) or trimellitic anhydride (TMA; a respiratory allergen). DNA from draining lymph nodes was processed for methylated DNA immunoprecipitation (MeDIP) followed by hybridization to a whole-genome DNA promoter array. 6319 differently methylated regions (DMR) were identified following DNCB treatment, while 2178 DMRs were measured following TMA treatment, with approximately half of the TMA DMR common to DNCB. When limited to promoter region-associated DMR, 637 genes were uniquely associated with DNCB induced DMR but only 164 genes were unique to TMA DMR. Promoter-associated DMR unique to either DNCB or TMA were generally hypomethylated whereas DMR common to both allergens tended to be hypermethylated. Pathway analyses highlighted a number of immune related pathways, including chemokine and cytokine signalling. These data demonstrate that chemical allergen exposure results in characteristic patterns of DNA methylation indicative of epigenetic regulation of the allergic response. Comparison of methylation profiles from allergens 2,4-dinitrochlorobenzene (DNCB; a contact allergen) and trimellitic anhydride (TMA; a respiratory allergen) or vehicle acetone:olive oil (AOO).
2014-02-07 | E-GEOD-54768 | biostudies-arrayexpress
Project description:Allergic asthma, a chronic disease-causing inflammation in the airways, is a significant public health concern. Our research team discovered that more than 80% of allergic children in central Taiwan were sensitized to various house dust mites (HDMs). This investigation focuses on how the crude extracts of HDMs affect human epithelium BEAS-2B cells to understand the early fundamental mechanisms for preventing allergic diseases. Therefore, RNA-seq analysis revealed that three Dermatophagoides HDMs allergens activate a common Toll-like receptor signaling pathway in human epithelial cells within a 4-hour treatment. During this process, the nuclear transcription factor NF-κB translocated into the cell nucleus within 30 minutes of allergen stimulation, triggering the expression of pro-inflammatory genes such as IL-6 and IL-8 over 4 hours. Additionally, treating the cells with specific Dermatophagoides microceras (Der m) allergens, there was an upregulation of genes in regulating type 1 diabetes mellitus signaling pathways, mediating IL-12A inflammation. Moreover, an increase in gene sets related to cilia function and the microtubule cytoskeleton in human epithelial cells following treatment combined with Der m allergens and Dexamethasone. Furthermore, OMICs analysis investigates the effects of HDMs allergenic stimulation on the human epidermal cells. This process aims to enhance our understanding of the cellular molecular mechanisms underlying potential targets and bioactive substances in precision medicine for treating asthma caused by HDMs allergens.
2023-12-31 | GSE243680 | GEO
Project description:IL-12 protects from psoriasiform skin inflammation
| PRJEB15422 | ENA
Project description:Epigenetic regulation of gene expression plays a pivotal role in the orchestration of immune responses and may determine the vigor, quality, or longevity of such responses. Chemical allergens can be divided into two categories: skin sensitizing chemicals associated with allergic contact dermatitis, and chemicals that cause sensitization of the respiratory tract and occupational asthma. In mice these are characterized by different T helper (Th) cell responses. To explore the regulation and maintenance of these divergent responses, mice were exposed to 2,4-dinitrochlorobenzene (DNCB; a contact allergen) or trimellitic anhydride (TMA; a respiratory allergen). DNA from draining lymph nodes was processed for methylated DNA immunoprecipitation (MeDIP) followed by hybridization to a whole-genome DNA promoter array. 6319 differently methylated regions (DMR) were identified following DNCB treatment, while 2178 DMRs were measured following TMA treatment, with approximately half of the TMA DMR common to DNCB. When limited to promoter region-associated DMR, 637 genes were uniquely associated with DNCB induced DMR but only 164 genes were unique to TMA DMR. Promoter-associated DMR unique to either DNCB or TMA were generally hypomethylated whereas DMR common to both allergens tended to be hypermethylated. Pathway analyses highlighted a number of immune related pathways, including chemokine and cytokine signalling. These data demonstrate that chemical allergen exposure results in characteristic patterns of DNA methylation indicative of epigenetic regulation of the allergic response.
2014-02-07 | GSE54768 | GEO
Project description:In naïve individuals, sensory neurons directly detect and respond to allergens, leading both to the sensation of itch and the activation of local innate immune cells, which initiate the allergic immune response1,2. In the setting of chronic allergic inflammation, immune factors prime sensory neurons, causing pathologic itch3-7. While these bidirectional neuroimmune circuits drive responses to allergens, whether immune cells regulate the set-point for neuronal activation by allergens in the naïve state is unknown. Here we describe a T cell-IL-3 signaling axis that controls the allergen responsiveness of cutaneous sensory neurons. We define a poorly characterized epidermal T cell subset8, termed GD3 cells, that produces its hallmark cytokine IL-3 to promote allergic itch and the initiation of the allergic immune response. Mechanistically, IL-3 acts on Il3ra-expressing sensory neurons in a JAK2-dependent manner to lower their threshold for allergen activation without independently eliciting itch. This T cell-IL-3 signaling axis further acts via STAT5 to promote neuropeptide production and the initiation of allergic immunity. These results reveal an endogenous immune rheostat that sits upstream of and governs sensory neuronal responses to allergens upon first exposure. This pathway may explain individual differences in allergic susceptibility and opens novel therapeutic avenues for treating allergic diseases.
2024-06-11 | GSE223220 | GEO
Project description:Basophils play critical roles in the development of mouse delayed-onset skin allergic inflammation (IgE-CAI model). Importantly, they also contribute to the resolution of allergic inflammation by promoting the generation of pro-resolving macrophages. However, it remains unclear how pro-resolving macrophages suppress excess inflammation. To address this, we conducted single-cell RNA-seq (scRNA-seq) analysis of the IgE-CAI skin lesion at days 3 and 5 post-challenge of allergens. scRNA-seq analysis identified four distinct monocyte-macrophage subpopulations, namely classical monoytes, early CMDMs, late CMDMs and resident-like macrophages. Based on the gene expression profiles, classical monoytes, early CMDMs, late CMDMs and resident-like macrophages corresponded to Ly6ChiPD-L2lo, Ly6ChiPD-L2hi, Ly6CloPD-L2hi, and Ly6CloPD-L2lo, respectively.
2024-01-22 | GSE245865 | GEO
Project description:Basophils play critical roles in the development of mouse delayed-onset skin allergic inflammation (IgE-CAI model). Importantly, they also contribute to the resolution of allergic inflammation by promoting the generation of pro-resolving macrophages. However, it remains unclear how pro-resolving macrophages suppress excess inflammation. To address this, we conducted single-cell RNA-seq (scRNA-seq) analysis of the IgE-CAI skin lesion at days 3 and 5 post-challenge of allergens. scRNA-seq analysis identified two distinct classical monocyte-derived macrophage (CMDM) populations, namely early and late CMDMs, in IgE-CAI skin lesion. The former population was preferentially observed at the peak of inflammation (day 3), whereas the latter one at the termination phase of inflammation (day 5). Gene ontology analysis revealed that genes associated with phagocytosis were enriched in late CMDMs. In particular, late CMDMs displayed upregulated expression of Gas6 and Mertk, key genes for phagocytic clearance of apoptotic cells. Taken together, scRNA-seq identified CMDMs that display high capacity of dead cell clearance and contribute to the resolution of IgE-CAI.
2024-01-22 | GSE221310 | GEO
Project description:Loss-of-function mutations in the filaggrin gene are heavily associated with the incidence and severity of atopic dermatitis. Moreover, filaggrin insufficiency in epidermal keratinocytes can lead to persistent allergic inflammation and an associated immune response suggesting a role for this protein in regulation of immunity. Here, we investigate how filaggrin insufficiency affects the gene expression pattern in a filaggrin-insufficient (shFLG) keratinocyte cell line HaCaT in response to stimulation with various inflammatory mediators and allergens.
2022-05-20 | GSE203409 | GEO
Project description:Current diagnostics for allergies, such as skin prick and radioallergosorbent tests, do not allow for inexpensive, high-throughput screening of patients. Additionally, extracts used in these methods are made from washed pollen that lacks pollen surface materials that may contain allergens. We sought to develop a high-throughput assay to rapidly measure allergen-specific IgE levels in sera and to explore the relative allergenicity of different pollen fractions (i.e. surface, cytoplasmic, commercial extracts). To do this, we generated a protein microarray containing surface, cytoplasmic, and commercial extracts from 22 pollen species, commercial extracts from nine non-pollen allergens, and five recombinant allergenic proteins. Arrays were incubated with <25uL of serum from 176 individuals and bound IgE was detected by indirect immunofluorescence, providing a high-throughput measurement of IgE levels.
2010-09-08 | E-MTAB-177 | biostudies-arrayexpress